CAJ | 학술논문

阿尔茨海默氏病（AD）是目前最常见的神经退行性疾病，主要表现为进行性的认知和记忆力下降，其发生、发展与星形胶质细胞在内的多种因素有关。近年来发现，星形胶质细胞可通过多种机制影响AD病理过程，如增加Aβ的产生及沉积、加速异常Tau蛋白的缠结、通过炎症因子加剧 Aβ的神经毒性、能量供应不足及神经递质释放障碍损害神经功能正常活动等。各个因素在 AD 不同阶段反复作用，互相影响，形成恶性循环，导致淀粉样斑块形成、神经元纤维缠结、突触减少及神经元丢失。保护星形胶质细胞的正常功能可能成为AD治疗的新靶点。
아이자해묵씨병（AD）시목전최상견적신경퇴행성질병，주요표현위진행성적인지화기억력하강，기발생、발전여성형효질세포재내적다충인소유관。근년래발현，성형효질세포가통과다충궤제영향AD병리과정，여증가Aβ적산생급침적、가속이상Tau단백적전결、통과염증인자가극 Aβ적신경독성、능량공응불족급신경체질석방장애손해신경공능정상활동등。각개인소재 AD 불동계단반복작용，호상영향，형성악성순배，도치정분양반괴형성、신경원섬유전결、돌촉감소급신경원주실。보호성형효질세포적정상공능가능성위AD치료적신파점。
To date, Alzheimer disease (AD), with the main clinical manifestations of progressive decline of cognitive and memory function, is the most common neurodegenerative disease, whose onset and development are closely associated with many factors including astrocytes. In recent years, many researches have indicated the role of astrocytes in the pathology of AD, for example, increasing the production and deposition of Aβ, accelerating the tangle of abnormal protein Tau, aggravating Aβneurotoxicity via inflammatory cytokines, lessening energy supply and compromising the normal neural activity caused by dysfunction of the transmitter release. In AD different pathological stages, these factors interact and form a vicious cycle, contributing to the formation of amyloid plaque and neurofibrillary tangle, synaptic reduction and neuronal loss. Recovery of the normal function of astrocytes in the early stage might be a potential therapeutic target for AD.